HALLUCINATIONS NATURAL VS DRUG-INDUCED Akshay Chandra

HALLUCINATIONS NATURAL VS. DRUG-INDUCED • Akshay Chandra • Jarrod Hyam • Maria Mann • Jenny Pranskevich

OUTLINE • Introduction • Maria – Natural Hallucinations • Jarrod – Mystical Hallucinations • Shay – Hallucinogens • Jenny – Conclusion

What is a Hallucination? • A hallucination is the brain's perception of a false sensory input • Experiencing of an event through one of their senses that is not occurring in the real world – – Visual Auditory (hearing one’s thoughts as if spoken aloud) Tactile Olfactory

CAUSES • Natural: • Meditation • Sensory Deprivation • Dreams • (Schizophrenia, Dementia, Exhaustion, Brain Tumors) • Drug Induced – – LSD DMT Mushrooms MDMA

Meditation During mediation the attention is brought into the field of the unconscious mind for extended periods of time. When the brain lacks external stimulation to form perceptions, it may compensate by referencing the memory and forming hallucinatory perceptions.

Meditation/Neural Correlates • Meditation is correlated with increased 5 HT Seratonin, a neuromodulator that influences the flow of visual associations generated by the temporal lobe. When 5 HT 2 receptors are activated, a hallucinogenic effect can result. 5 HT inhibits the LGN, reducing the amount of visual info that passes through. • When combined with reticular nucleus inhibition, 5 HT may increase the fluidity of temporal visual associations in the absence of sensory input.

Sensory Deprivation If one eliminates external sources of low-level pain and sources of danger, the inner experience can be anything one allows itself to experience.

Hallucinations & Dreams • Hypnagogic hallucinations are short, usually auditory hallucinations that occur when a person is falling asleep. • Hypnopompic hallucinations occur when a person is waking up.

Dreams/Neural Correlates • When relative activation of 5 HT 2 to 5 HT 1 was reduced, REM sleep was suppressed. Therefore, relative activation of 5 HT 2 pathways are implicated in REM sleep. The subjective experience of dreaming is likely a result of 5 HT 2 activation, much like the pathway responsible for the effects of etheogenic drugs.

Perception Hallucination Continuum Both natural and drug induced states are marked by a gradual turning inward toward a mental dimension at the expense of the physical.

Left-Right Hemispheric Switch Data processing is preferentially shifted to the visuospatial, right hemisphere when one departs on the perceptionhallucination continuum naturally or via hallucinogenic drugs.

Mystical States • Specific form of hallucinatory experience • Main characteristics are: 1. ) Ecstatic mood 2. ) Sense of newly gained knowledge about reality 3. ) Perceptual alterations 4. ) No sense of space or time 5. ) Unity with all of life

Good Friday Experiment - Pahnke • Investigated the potential of hallucinogens to facilitate mystical experience • Double-blind experiment: –Twenty theology students, who had never taken psilocybin given either placebo or 30 mg psilocybin during a Good Friday Church Service

PSILOCYBIN •

• A questionnaire was given after the experiment • Subjects in the control group reported: a. ) 5% internal unity, 1% external unity b. ) 7% transcendence of time and space c. ) 23% deeply felt positive mood • Experimentals reported: a. ) 60% internal unity, 39% external unity b. ) 78% transcendence of time and space c. ) 54% deeply felt positive mood

Neurochemical Theory for Mystical States • Synthesis of endogenous hallucinogen 5 methoxy-dimethyltryptamine (DMT) from the pineal gland • DMT is Part of the Tryptamine Family: – Tryptamines are alkaloids with an indole structure – Other hallucinogenic tryptamines include LSD and psilocybin – These compounds have a cultural context of mystical-state induction

Hallucinogens LSD (Lysergic Acid Diethylamide) MDMA (3, 4 -methylenedioxymethamphetamine ) 2 -CB (4 -bromo-2, 5 -dimethoxyphenethylamine ) Psylocybin (Mushrooms)

MDMA Dosage: 80 -150 mg Onset: 30 – 60 minutes Duration: 3 – 4 hours (if taken orally) Effect: emotional openness, euphoria, stimulation, reduction of critical and cynical thoughts, and decrease of inhibitions few prominent open or closed eye visuals, only a small percent report significant visual distortions.

2 C-B Dosage: 10 – 40 mg Onset: 45 – 75 minutes Duration: 4 – 6 hours Effect: a wide variety of perceptual changes may occur; pupil dilation, visual patterning and movement, mental stimulation, new perspectives, feelings of insight, emotional shifts (mood lift or introspection), anxiety and confusion

Psilocybin Dosage: 1 -5 grams of dried mushrooms Onset: 30 - 60 minutes Duration: effects last 4 - 6 hours Effects: pupil dilation, visuals, mental stimulation, new perspectives, feelings of insight, quickly changing emotions (lots of laughter), possible paranoia and confusion

LSD Threshold: 20 micro grams Dosage: 50 - 150 micro grams Onset: 30 – 120 minutes Duration: 6 – 14 hours

Effect - In the beginning stages: feeling similar to anticipation or anxiety, a slight feeling of energy in the body, an extra twinkle to lights, or the feeling that things are somehow different than usual. - As the effects become stronger: non-specific mental and physical stimulation, pupil dilation, closed and open eye patterning and visuals, changed thought patterns, feelings of insight, confusion, or paranoia, and quickly changing emotions.

Neurological effect • Ungerleider and Pechnick concluded that LSD and similar hallucinogenic agents work by an agonist effect at the 5 HT 2 receptor • LSD not only has affinities for 5 -HT receptors but also for receptors of histamine, ACh, dopamine, and the catecholines: epinephrine and norepinephrine LSD binding at 5 -HT 2 receptor

Receptors and brain physiology • convergent evidence shows that there is a high concentration of 5 -HT-2 receptors, and of hallucinogen binding in the claustrum • The V 1 target zone in the claustrum appears to overlap to some degree with those of higher order visual areas, which are specialized for the processing of motion, color, and form, and with areas of parietal and prefrontal cortex that have been implicated in attention, working memory, and the generation of eye movements

Potential explanation for LSD hallucinations • integrity of the visual cortico-claustral loop may be necessary for precise temporal integration of edge information from end-inhibited and line-detector cell populations, and that the nature of this temporal coding may be modulated based on the expected motion of objects, eye movements, and selective attention. • Therefore, the dysfunction of inhibition in these areas caused by psychedelics may, at least in part, mediate the visual distortions they produce.

CONCLUSIONS • THEORIES – Serotonin and 5 -HT 2 Receptors • Indole Rings – Sensory overload • Visual hallucinations not produced in patients who have a severed optic nerve

SEROTONIN PATHWAYS • serotonin pathways innervate different brain regions. • the Raphe nucleus – long axons project to higher centers in the brain including the neocortex and the limbic system (e. g. , the amygdala and hippocampus • Second pathway that goes down brainstem

SEROTONIN RECEPTORS • Serotonin has several classes of different binding sites • 5 HT 1 Receptors: Regulates serotonin levels • 5 HT 2 Receptors: stress management • 5 HT 3 Receptors: “Happiness”

5 -HT 2 Receptors • Found on the post-synaptic neuron • G-protein-coupled • Typically inhibited by hallucinogenic drugs – More difficult to generate an action potential

INDOLE RINGS • M Serotonin Mescaline LSD Psylocibin

DRUGS DON’T DO ANYTHING TO THE BRAIN THAT THE BRAIN CANT DO TO ITSELF

RESOURCES • Altman, Christopher. “Neuropharmacology of the Mystical State. ” http: //artilect. org/altman/mysticism. html May 30, 2005 • Bourgeois, James, De. Juan Thomas, Johansem Thomas, and David Walker. “Visual Hallucinations Associated With Fluoxetine and Sertraline. ” Journal of Clinical Psychopharmacology: 18(1998): 482 -483 • Doblin, Rick. “Pahnke’s ‘Good Friday Experiment’: A Long-Term Follow-Up and Methodological Critique. ” The Journal of Transpersonal Psychology. 23 (1990) • Ffytche, Dominic. “Visual Hallucination and Illusion Disorders: A Clinical Guide. ” Advances in Clinical Neuroscience and Rehabilitation. 2004. (4) 16 -18. Frith, Chris, and Ray Dolan. “The Role of the Prefrontal Cortex in Higher Cognitive Functions. ” Brain and Cognition. 5 (1996): 175 -181. • May 30, 2005 • May 30, 2005 May 30, 2005 • May 30, 2005 • May 30, 2005 • Newberg, Andrew B. & Iversen, J. “The neural basis of the complex mental task of meditation: neurotransmitter and neurochemical considerations. ” Medical Hypotheses. 2003. 61(2), 282 -291. • Ramachandran, V. S. and R. L. Gregory (1991). Perceptual filling in of artificially induced scotomas in human vision. Nature, 350, 699.

RESOURCES CONT. • Scott, Foresman. Behavioral Analysis of Drug Action. Ed. John A. Harvey. Glenview, Illinois, 1971. • Siegle, Ronald. Fire in the Brain: Clinical Tales of Hallucination. New York: Penguin Books, 1992. • Siegle, Ronald, and L. J. West. Hallucinations: Behavior, Experience, and Theory. New York: John Wilsey & Sons, 1975. • Wallace, Benjamin and Leslie Wallace. Consciousness and Behavior 4 th Ed. Prospect Heights: Waveland Press, 1999.